ArticleCell death and differentiation2014
Microglia convert aggregated amyloid-β into neurotoxic forms through the shedding of microvesicles.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
172 citing papers in PubMed, 271 citations in OpenAlex.
- Towards a systematic understanding of the diverse subtypes, biogenesis and functions of large extracellular vesicles.Nature reviews. Molecular cell biology · 2026Review
- Microglia-derived extracellular vesicle content as a biomarker for early detection of Alzheimer's disease.Translational neurodegeneration · 2026Review
- Low-Sample Input miRNA Profiling in Extracellular Vesicles-Enriched Plasma Fractions from Older Adults With/out Cognitive Impairment.International journal of molecular sciences · 2026Article
- Microglial mitophagy as an immunometabolic checkpoint in alzheimer's disease: linking mitochondrial quality control to neuroinflammation.Journal of neuroinflammation · 2026Review
- Vespakinin-M delineates an AMPK/mTOR-arginine-TCA cycle axis to act as an immunometabolic switch in post-stroke microglia.Redox biology · 2026Article
- Small Extracellular Vesicles from Neural Cells: Physiological and Pathological Roles, and Potential in Neurodegenerative Therapy.Advanced healthcare materials · 2026Review
- Glycolysis: The Bridge Between Cellular Interaction and Alzheimer's Disease.Biomolecules · 2026Review
- Glial Cells in the Early Stages of Neurodegeneration: Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 2025Review
- Lipid and lipoprotein metabolism in microglia: Alzheimer's disease mechanisms and interventions.Journal of lipid research · 2025Review
- Listerin Alleviates Alzheimer's Disease through IRE1-mediated Decay of TLR4 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Multifaceted Role of Extracellular Vesicles in Alzheimer's Disease.Journal of neurochemistry · 2025Review
- Mechanisms of Action of Propofol in Modulating Microglial Activation in Ischemic Stroke.Molecules (Basel, Switzerland) · 2025Review
- Depression exacerbates AD pathology through lactate-dependent activation of microglial Kv1.3 to promote Aβ-containing exosome spreading.Journal of neuroinflammation · 2025Article
- Unveiling the Involvement of Herpes Simplex Virus-1 in Alzheimer's Disease: Possible Mechanisms and Therapeutic Implications.Molecular neurobiology · 2025Review
- Extracellular particles: emerging insights into central nervous system diseases.Journal of nanobiotechnology · 2025Review
- Roles, Functions, and Pathological Implications of Exosomes in the Central Nervous System.International journal of molecular sciences · 2025Review
- The Role of Small Extracellular Vesicles Derived from Glial Cells in the Central Nervous System under both Normal and Pathological Conditions.Neurochemical research · 2025Review
- Elevated Serum Extracellular Vesicle-Packaged SPARC in Hypertension: A Cross-Sectional Study in a Middle-Aged and Elderly Population.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Microglial CD2AP deficiency exerts protection in an Alzheimer's disease model of amyloidosis.Molecular neurodegeneration · 2024Article
- Extracellular vesicles: biological mechanisms and emerging therapeutic opportunities in neurodegenerative diseases.Translational neurodegeneration · 2024Review
112 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by extracellular amyloid-β (Aβ) deposition, which activates microglia, induces neuroinflammation and drives neurodegeneration. Recent evidence indicates that soluble pre-fibrillar Aβ species, rather than insoluble fibrils, are the most toxic forms of Aβ. Preventing soluble Aβ formation represents, therefore, a major goal in AD. We investigated whether microvesicles (MVs) released extracellularly by reactive microglia may contribute to AD degeneration. We found that production of myeloid MVs, likely of microglial origin, is strikingly high in AD patients and in subjects with mild cognitive impairment and that AD MVs are toxic for cultured neurons. The mechanism responsible for MV neurotoxicity was defined in vitro using MVs produced by primary microglia. We demonstrated that neurotoxicity of MVs results from (i) the capability of MV lipids to promote formation of soluble Aβ species from extracellular insoluble aggregates and (ii) from the presence of neurotoxic Aβ forms trafficked to MVs after Aβ internalization into microglia. MV neurotoxicity was neutralized by the Aβ-interacting protein PrP and anti-Aβ antibodies, which prevented binding to neurons of neurotoxic soluble Aβ species. This study identifies microglia-derived MVs as a novel mechanism by which microglia participate in AD degeneration, and suggest new therapeutic strategies for the treatment of the disease.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.